Voiding dysfunction in women: How to manage it correctly A. Abdel Raheem

Arab Journal of Urology (2013) 11, 319–330
Arab Journal of Urology
(Ofﬁcial Journal of the Arab Association of Urology)
www.sciencedirect.com
VOIDING DYSFUNCTION/FEMALE UROLOGY
REVIEW
Voiding dysfunction in women: How to manage
it correctly
A. Abdel Raheem a, Helmut Madersbacher
a
b
b,*
Department of Urology, Tanta University Hospital, Egypt
Department of Neurology, Medical University Innsbruck, Austria
Received 20 April 2013, Received in revised form 3 July 2013, Accepted 13 July 2013
Available online 30 August 2013
KEYWORDS
PVR measurement;
Bladder diary;
Uroﬂowmetry;
Women
ABBREVIATIONS
VD, voiding dysfunction;
DU, detrusor underactivity;
DO, detrusor overactivity;
DM, diabetes mellitus;
PVR, postvoid residual
urine volume;
Qmax, maximum urinary ﬂow rate;
Abstract Introduction: Of women aged >40 years, 6% have voiding dysfunction
(VD), but the deﬁnition for VD in women with respect to detrusor underactivity
(DU) and bladder outlet obstruction (BOO) is not yet clear. In this review we
address the current literature to deﬁne the diagnosis and treatment of VD more accurately.
Methods: We used the PubMed database (1975–2012) and searched for original
English-language studies using the keywords ‘female voiding dysfunction’, ‘detrusor
underactivity’, ‘acontractile detrusor’ and ‘bladder outlet obstruction and urinary
retention in women’. We sought studies including the prevalence, aetiology, pathogenesis, diagnosis and treatment of female VD.
Results: In all, 20 original studies were identiﬁed using the selected search criteria,
and another 45 were extracted from the reference lists of the original papers. All
studies were selected according to their relevance to the current topic and the most
pertinent reports were incorporated into this review.
Conclusion: Female VD might be related to DU or/and BOO. Voiding and storage symptoms can coexist, making the diagnosis challenging, with the need for a targeted clinical investigation, and further evaluation by imaging and urodynamics. To
date there is no universally accepted precise diagnostic criterion to diagnose and
* Corresponding author. Address: Department of Neurology, Medical University, Anichstraße 35, A-6020 Innsbruck, Austria. Tel.: +43
6643411645.
E-mail address: [email protected] (H. Madersbacher).
Peer review under responsibility of Arab Association of Urology.
Production and hosting by Elsevier
2090-598X ª 2013 Production and hosting by Elsevier B.V. on behalf of Arab Association of Urology.
http://dx.doi.org/10.1016/j.aju.2013.07.005
320
Pdet, detrusor pressure;
Pdetmax, maximum
Pdet;
PdetQmax, Pdet at
Qmax;
ApBO, acute prolonged bladder overdistension;
POP, pelvic organ
prolapse;
MUS, mid-urethral
sling;
TVT, tension-free
vaginal tape;
DV, dysfunctional
voiding;
DSD, detrusor sphincter dyssynergia;
PFM, pelvic ﬂoor
muscles;
US, ultrasonography;
PFS, pressure-ﬂow
study;
EMG, electromyography;
VCUG, voiding cystourethrogram;
IVES, intravesical
electrical stimulation;
CIC, clean intermittent
self-catheterisation;
SNM, sacral neuromodulation;
BTA, botulinum toxin
A
Abdel Raheem, Madersbacher
quantify DU and BOO in women. For therapy, a complete cure might not be possible for patients with VD, therefore relieving the symptoms and minimising the
long-term complications associated with it should be the goal. Treatment options
are numerous and must be applied primarily according to the underlying pathophysiology, but also considering disease-speciﬁc considerations and the abilities and
needs of the individual patient. The treatment options range from behavioural therapy, intermittent (self-)catheterisation, and electrical neuromodulation and neurostimulation, and up to urinary diversion in rare cases.
ª 2013 Production and hosting by Elsevier B.V. on behalf of Arab Association of
Urology.
Introduction
Voiding dysfunction (VD) in women is a common
health problem and can be related to either an abnormality in detrusor muscle activity and/or BOO. In a
large cross-sectional Internet survey including 15,861
women aged >40 years in the USA, UK and Sweden,
terminal dribbling was the most common symptom in
38.3%, followed by a feeling of incomplete bladder emptying in 27.4% and a weak stream in 20.1% [1]. In the
standardisation of terminology of LUTS there is a lack
of consensus about a precise diagnosis and deﬁnition of
voiding abnormalities. Storage and voiding symptoms
can coexist, which might have an independent pathophysiology or be related to one another [2]. This makes
female VD a challenge in clinical practice, to obtain the
precise diagnosis and choose the best and most suitable
treatment.
In this review we address what is considered as VD in
females, identify the causes, and suggest possible diagnostic and therapeutic strategies.
Methods
We used the PubMed database (1975–2012) and
searched for original English-language studies using
the keywords ‘female voiding dysfunction’, ‘detrusor
underactivity’, ‘acontractile detrusor’, ‘urinary retention’ and ‘bladder outlet obstruction’ in women. In all,
20 original studies were identiﬁed using the selected
search criteria, and a further 44 were extracted from
the reference lists of the original papers. We assessed
studies concerned with the prevalence, aetiology,
pathogenesis, diagnosis and treatment of female VD.
The most pertinent 65 reports are the basis for this
article.
Voiding dysfunction in women: How to manage it correctly
Aetiology of female VD
VD is used to describe a clinical condition that affects
bladder emptying. The causes can be related to either
detrusor underactivity (DU) or acontractility, and/or
BOO (Table 1).
Abnormal detrusor muscle activity
The ICS deﬁnes DU as ‘a contraction of reduced
strength and/or duration, resulting in prolonged bladder
emptying and/or failure to achieve complete bladder
emptying within a normal time span’, while an acontractile detrusor is deﬁned as one ‘which cannot be demonstrated to contract during urodynamic studies’ [3].
‘Primary’ or ‘idiopathic’ DU is thought to be an agerelated decrease in detrusor contractility with no other
causes, while secondary DU is associated with a
Table 1
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detectable relevant condition, e.g., diabetes mellitus
(DM) or BOO [4]. The pathogenesis of DU can be myogenic or neurogenic.
Neurogenic factors
Cerebral (especially pontine), spinal sacral and subsacral
lesions can cause DU or acontractile detrusor (Table 1).
The patient’s symptoms and urodynamic presentations
vary according to the location and extension of the lesion,
and might change during disease progression, e.g., in the
early stages of multiple sclerosis, overactive bladder
symptoms are common, but in late stages chronic voiding
problems prevail. The prevalence of DU in multiple sclerosis is 0–40%, and 25% in the earlier stage. Later in the
disease 25% of patients had chronic urinary retention
with an increased postvoid residual urine volume (PVR)
due to detrusor weakness and/or functional BOO [5].
The causes of female VD.
Condition
Type
Detail
(1) Abnormal detrusor activity
(underactive/acontractile)
Neurogenic
Cerebral:
Cerebrovascular stroke
Multiple sclerosis
Multiple system atrophy
Hydrocephalus
Tumour (brain, spinal cord)
Spinal (sacral):
Spinal cord injury
Disc herniation
Transverse myelitis
Spina biﬁda
Subsacral (peripheral):
Pelvic nerve injury (iatrogenic – traumatic)
Ageing
ApBO
DM
Menopause
Immobility
Recurrent UTI
Anaesthesia
Post operative
Drugs
Psychological
Myogenic
Mixed
Other risk factors
(2) BOO
Anatomical
Functional
Iatrogenic obstruction:
Anti-incontinence (sling) procedures
Urethral procedures
POP
Anterior vaginal wall prolapse
Apical prolapse (procedentia)
Inﬂammatory process:
Inﬂammation of urethra
Urethral stricture
Urethral diverticulum
Miscellaneous:
Bladder calculi/tumour
Retroverted uterus
Female genital tumours
Dysfunctional voiding
DSD
Fowler’s syndrome
322
Impaired detrusor contractility is very frequent in patients with multiple system atrophy. It is present in 58%
of patients within the ﬁrst 4 years and in 76% during the
course of the disease [6], often combined with detrusor
overactivity (DO), leading clinically to an increased
PVR, urgency and urgency incontinence. The urological
symptoms can be the ﬁrst sign of the disease.
In stroke patients, DU was found in up to 40% [7]. It
appears to be more common in patients with pontine
strokes rather than in those with fronto-parieto-temporal lesions.
DU can result from iatrogenic nerve damage after
radical pelvic surgery, due to peripheral, mostly partial,
sympathetic and parasympathetic denervation. More
than half of women with a normal urinary tract function
before surgery have voiding problems after a radical
hysterectomy, at least temporarily, using either abdominal straining or needing catheterisation [8]. VD occurs
in a third of patients treated for rectal cancer, with a
higher risk in low rectal cancer and abdominoperineal
resection [9].
Myogenic factors
The ageing process is a common but not the only reason
for detrusor weakness. It can cause degenerative detrusor weakness, and affect the detrusor’s ability to maintain a sustained contraction to empty the bladder
completely. However, the results are not uniform. In a
study of men and women aged >70 years, impaired
detrusor contractility was detected in 48% of men and
12% of women [10]. Madersbacher et al. [11] studied
the urodynamic changes with ageing in women and
showed a signiﬁcant decrease (P < 0.05) in maximum
urinary ﬂow rate (Qmax), voided volume, bladder capacity, maximum urethral closing pressure, functional urethral length and an increased PVR, but there were no
signiﬁcant age-associated changes for maximum detrusor pressure (Pdetmax), detrusor pressure at Qmax
(PdetQmax), and incidence of DO. Resnick and Yalla
[12] found, among institutionalised elderly people with
urinary incontinence, that 33% had DO with an impaired contractile function.
Acute prolonged bladder overdistension (ApBO) is
an important, but often unrecognised medical phenomenon and occurs after extensive pelvic surgery, operations with spinal anaesthesia and prolonged childbirth.
Silent postpartum urinary retention affects 37% of women, with a PVR of >150 mL [13]. The pathogenesis of
ApBO probably comprises two consecutive stages, i.e., a
primary temporary neurogenic dysfunction leading to
acute urinary retention, that if neglected will be followed
by secondary myogenic detrusor damage. Recovery depends on whether there is reversible or irreversible damage [14].
Abdel Raheem, Madersbacher
Mixed (neurogenic and myogenic) factors
A good example of this is ‘diabetic cystopathy’, a term
ﬁrst introduced by Frimodt-Moller [15], to describe
LUTS associated with DM. An abnormal bladder function with DM is traditionally attributed to peripheral
autonomic neuropathy leading to impaired sensation,
with consequent bladder overdistension, decreased ﬂow
rates and an increased PVR. However, detrusor smooth
muscle cells can also be modulated directly by hyperglycaemia, which induces oxidative stress in muscle cells,
with macro- and micovascular damage. The latter might
have a similar effect on the diabetic bladder as defects
seen with retinopathy and nephropathy [16]. Lee et al.
[17] reported the early urodynamic ﬁndings of diabetic
bladder dysfunction in women; there was DU in
34.9%, DO in 14% and BOO in 12.8%, but BOO was
due to a comorbidity of other origin.
Other risk factors
Other risk factors can also contribute to DU, e.g., menopause [18], constipation [19], immobility, anaesthesia,
and recurrent UTI. Menopause can result in axonal
degeneration and loss of detrusor muscle cells, while
constipation leads to rectal distension, reﬂexively
decreasing detrusor contractility and/or obstructing the
bladder outlet due to faecal impaction.
A broad range of medication is known to contribute
or to cause VD, e.g., antipsychotics, anticholinergics,
antidepressants, some antiparkinsonian drugs (apomorphine), opiates, antihistamines and adrenergic agonists.
Boo
The causal factors for female BOO are either anatomical
or functional (Table 1).
Anatomical
Pelvic organ prolapse (POP), such as a high-grade cystocele or uterine prolapse, can lead to ‘mechanical’ BOO.
This occurs in 2% of women with grades 1 and 2 POP,
and up to 33% with grades 3 and 4 POP [20]. A cystocele can cause kinking of the urethra, and moreover, a
large amount of the energy created by detrusor contraction is lost due to inadequate pressure transmission from
the bladder to the urethra.
De novo VD has been reported after placing mid-urethral slings (MUS). The reported rate after placing a
tension-free vaginal tape (TVT) is 3–15% [21]. The transobturator tape was associated with similar rates of VD
as the TVT, with a signiﬁcant decrease in Qmax from 30
to 20 mL/s (P = 0.001) and a signiﬁcant increase in
PVR from 13 to 43 mL (P = 0.03) [22].
Voiding dysfunction in women: How to manage it correctly
Urethral strictures can result from urethral inﬂammation, traumatic urethral injury or iatrogenic trauma due
to recurrent urethrotomies or long-term catheterisation.
Functional
Causes for functional BOO are dysfunctional voiding
(DV) and detrusor sphincter dyssynergia (DSD). Other
rare causes include Fowler’s syndrome and a primary
bladder neck obstruction.
The ICS [3] deﬁned DV as ‘an involuntary intermittent contraction of the peri-ureteral striated muscle during voiding in neurologically intact individuals’, a
phenomenon ﬁrst described by Hinman [23], while
DSD is deﬁned as ‘a detrusor contraction concurrent
with an involuntary contraction of the striated urethral
sphincter/pelvic ﬂoor muscle in neurogenic patients’.
Hinman syndrome (a non-neurogenic neurogenic
bladder) is also termed an ‘acquired voiding dysfunction’. Hinman suggested that this VD is caused by faulty
learned behaviour as patients attempt to inhibit micturition by voluntary contraction of the external urethral
sphincter/pelvic ﬂoor muscles (PFM), which can be reversed with re-educational therapy.
Fowler and Kirby [24] described the electrophysiological responses of the urethral rhabdosphincter in
young women with unexplained urinary retention, using
a needle electrode, and reported abnormal electromyographic activity (complex repetitive discharges and
decelerating bursts). The typical clinical presentation
of Fowler’s syndrome is a young female patient presenting with painless urinary retention (PVR > 1 L), pain
during catheter withdrawal and no evidence of urological or neurological disease. Investigations showed an
abnormally high urethral pressure proﬁle and an increased sphincter volume on ultrasonography (US).
Up to 40% of these patients have polycystic ovary disease, with the hypothesis that a hormonal abnormality
might affect sphincter activity.
The diagnosis of female VD
In women with VD, the voiding and storage symptoms
can coexist, making the diagnosis even more challenging. Thus they must be accurately evaluated with urodynamic and imaging studies, to obtain a precise diagnosis.
Symptoms and signs
VD symptoms include hesitancy, weak stream, intermittency, straining to void, spraying or a split stream,
incomplete bladder emptying, a need to immediately
re-void, position-dependent micturition and postmicturition dribbling. Sometimes women complain of concomitant stress and/or urge urinary incontinence.
Storage-related symptoms such as frequency, urgency
323
and nocturia might be present, either due to an increased PVR or associated comorbidity [2].
Urinary retention, painless or painful, and acute or
chronic, might be present. In acute retention, patients
are unable to pass urine and on examination have a palpable or percussible bladder. Chronic retention has a
more insidious presentation and patients complain of
frequency, weak stream, overﬂow incontinence or recurrent UTI.
In females with VD the predictive value of voiding
symptoms is rather low, e.g., for the PVR the sensitivity
is 13–57%, and the speciﬁcity 18–38% [25,26]. Kuo [27]
concluded that clinical symptoms alone are not reliable
in the differential diagnosis of LUTS in women. Thus it
is very important for physicians to know that the diagnosis of female VD depends both on the patient’s symptoms and the ﬁnal investigational results, including a
urodynamic study.
Physical examination
Suprapubic fullness can be present during an abdominal
examination. A pelvic examination can show vaginal
atrophy, vulvo-vaginitis, POP or pelvic masses. Palpation of the urethra and anterior vaginal wall can detect
urethral tenderness, a diverticulum or scarring. A
DRE can be used to diagnose faecal impaction, assess
the anal sphincter tone and the ability to contract voluntarily the anal sphincter. The spinal reﬂex activity of L5–
S5 is assessed by testing the bulbocavernosus reﬂex
(squeezing of the clitoris induces anal sphincter contraction), and the spinal reﬂex activity of the S4–S5 nerve
roots by anal reﬂex testing.
Urine analysis and urine culture
UTI in women has been reported to be associated with
VD; up to 42% of female patients with VD had a history
of recurrent UTI [28].
US can be used to estimate the PVR, bladder wall
thickness, and to identify any associated pathologies,
e.g., bladder stone or diverticulum [29].
Non-invasive urodynamic testing
A bladder diary recorded for 2 days [30] or 3–7 days [31]
provides objective data on ﬂuid intake, the frequency of
micturition, total voided volume, maximum voided volumes and incontinence episodes.
Uroﬂowmetry shows a prolonged and either continuous, ﬂuctuating or interrupted pattern with no peak
(plateau pattern) with a decreased maximum and mean
ﬂow rate (Fig. 1). However, uroﬂowmetry alone cannot
distinguish between DU and BOO, so pressure-ﬂow
studies (PFS) are necessary [32].
324
The PVR can be estimated using US or catheterisation. According to Abrams et al. [32], VD in women is
associated with a PVR of >30% of the functional bladder capacity.
Invasive urodynamic studies
If noninvasive urodynamic testing detects abnormalities,
to distinguish between DU and BOO, invasive urodynamic tests, especially PFS, are necessary. Urodynamic
studies can be combined with video-cystography (video-urodynamics) and electromyography (EMG) of
the PFM/striated sphincter.
Abdel Raheem, Madersbacher
difﬁculties is much lower when an adequate detrusor
contraction is present.
Despite all these studies there is still no agreement
and a lack of consensus on the precise determination
and deﬁnition of female VD based on urodynamic
variables.
The voiding cysto-urethrogram (VCUG)
The VCUG provides important information about the
morphology and function of the lower urinary tract
and is essential for locating an infravesical obstruction.
It can be done either alone (Fig. 1) or combined with
urodynamics (VUD).
Urodynamic challenges in the diagnosis of female VD
EMG of the PFM and the striated sphincter
There is no universally accepted precise diagnostic criterion to diagnose and quantify DU and/or BOO in women [2]. Algorithms, which have been developed to
quantify detrusor power during voiding, like the Grifﬁths Watt factor [33], Schafer’s nomogram [34] and
bladder contractility index [35] are validated for adult
men but not for women [4]. There is only one validated
nomogram for women, the Blavais–Groutz nomogram
[36], but it does not reﬂect all ﬁndings about BOO and
detrusor contractility. Moreover, in several other studies
the urodynamic criteria were evaluated for BOO in women. The values of both Qmax (mL/s) and PdetQmax (cm
H2O) were different, with mean or mean (SD) values of
PdetQmax of P35 [37], 37.2 (19.2) [36], 42.8 (22.8) [38]
and P60 [39] reported, with relevant values of Qmax of
615 [37], 9.4 (3.9) [36], 9 (6.2) [38] and 615 [39], respectively. Taking these different values into account we suggest that a PdetQmax of P40 cm H2O and a Qmax of
615 mL/s are indicative of BOO (Fig. 1).
The diagnosis of DU is often difﬁcult in women as
they void at a very low detrusor pressure (Pdet). This
could be because they have a low urethral resistance
due to perfect relaxation of the PFM and/or due to a
weak bladder outlet. With this situation there is no need
for the detrusor to accumulate relevant pressures [35].
Some women showed no appreciable increase in Pdet
during voiding and accordingly no diagnosis of DU
could be made. However, when the bladder neck is
blocked by balloon inﬂation of the urodynamic catheter
and voiding is repeated, then the Pdet might increase
considerably, indicating that the detrusor is capable of
producing a pressure, and the main cause of a low Pdet
in routine PFS is the absence of urethral resistance. This
can also be shown in some women when they are asked
to interrupt the stream during voiding, but this is not always possible due to sphincter weakness. Therefore this
test is less reliable than bladder neck blocking (Fig. 2).
The ﬁnding of a forceful detrusor contraction with a
blocked bladder neck has prognostic value. When
implanting a sling the risk of postoperative voiding
Mostly, EMG of the PFM is recorded using self-adhesive electrodes. Increased activity of the PFM during
voiding or nonrelaxation can be documented with
EMG, which can be combined with PFS (PFS–EMG).
This gives additional information and is useful to differentiate between a functional and structural obstruction.
Endoscopy
Cysto-urethroscopy, including calibration of the meatus
and urethra, gives additional information about the
cause of BOO and the consequences of infravesical
obstruction. However, bladder wall trabeculation is
not necessarily a sign of infravesical obstruction. Trabeculation not related to BOO related can occur with
infection, DO and chronic overdistension.
The treatment of female VD
Different therapeutic options are available to treat female VD, depending on the ﬁnal diagnosis and whether
the target is the detrusor, the bladder outlet or both.
Prevention and care after surgery
The early recognition of urinary retention after major
surgery and labour might avoid the long-term problems
associated with ApBO. This emphasises the importance
of strict postoperative voiding surveillance, with measurements of PVR using US, and just to assess voiding
volumes without an estimate of PVR is not sufﬁcient.
Nerve-sparing techniques for radical pelvic surgery,
preserving the pelvic autonomic nerves, are more
favourable in terms of an early return of bladder function [40,41].
Treatment of DU
The treatment of women with DU should target either
increasing bladder contractility, decreasing outﬂow
Voiding dysfunction in women: How to manage it correctly
resistance, or both [4]. There are several treatment options available.
Behavioural therapy
Women with DU should ﬁrst be offered behavioural
therapy, comprising lifestyle modiﬁcations and bladder
training, especially voiding at regular intervals to avoid
bladder overdistension. Constantinou et al. [42] presented the concept of ‘optimum ﬁlling volume for minimum bladder work’ and showed that with an adequate
bladder ﬁlling volume of 300–350 mL the detrusor contraction is most effective. Assisted voiding by abdominal
straining is an option for women who are able to relax
their PFM while straining to void. With double- and triple-voiding, about 20 min after micturition the patient
should try again to empty the bladder, so the PVR can
be reduced gradually.
Pharmacotherapy
Drug treatment for VD mostly includes muscarinic
receptor agonists (e.g. bethanechol) or cholinesterase
inhibitors (e.g. distigmine). However, there are no studies conﬁrming that parasympathicomimetics are able to
induce or reinforce detrusor contractions [43]. Nevertheless, they might have the clinical effect that the sensation
of bladder fullness is recognised earlier by increasing the
muscle tone of the bladder, and are therefore a beneﬁt
for some patients.
Another target is to decrease outﬂow resistance using
a-blockers, which can facilitate voiding but have the
danger of inducing or increasing stress urinary
incontinence.
Intravesical electrical stimulation (IVES)
IVES can be used to improve bladder dysfunction by
stimulating A-d mechanoreceptor afferents. To be effective IVES should be applied only if at least some functioning afferent ﬁbres between the bladder and the
cortex are still intact, and the detrusor muscle can still
contract [44]. IVES proved to have a role in detrusor
reinforcement in ApBO; up to two-thirds of patients
with a weak detrusor regained balanced voiding [45].
Of patients with incomplete spinal cord injury and
who had chronic neurogenic non-obstructive urinary
retention, 37.2% responded to IVES and 83.3% experienced again the sensation of bladder ﬁlling [46].
Clean intermittent self-catheterisation (CIC)
If there is a signiﬁcant PVR that cannot be abolished or
lowered otherwise, CIC is indicated. This should be
timed to every 4–5 h, encouraging the patient to use
abdominal Valsalva and positional techniques to empty
325
the bladder completely while the catheter is in the bladder. Others prefer the CIC frequency to depend on the
voided volume and PVR, with both together not
>600 mL. CIC is still the standard treatment of choice
for DU and is also suitable for long-term care [47].
Indwelling catheterisation is a last resort for women
with VD in whom all other treatments have failed or
who are unable to use CIC regularly, with a preference
for a suprapubic over a urethral catheter, as there is a
lower incidence of contamination. CIC and especially
indwelling catheterisation can compromise the quality
of life in some patients.
Sacral neuromodulation (SNM)
Although the exact mechanism of action of SNM is still
not well understood, several mechanisms of action have
been postulated, such as the correction of a disturbed reﬂex action, or using a ‘rebound’ phenomenon in the
CNS through afferent pathway stimulation to the brain
area that controls bladder and sphincter function.
Therefore, to our knowledge, electrical neuromodulation should not work in patients with a complete spinal
cord injury [4]. Moreover, SNM can only work if the
detrusor is still able to contract, so a chronically overdistended bladder with recurrent UTI, and therefore a
large ﬁbrotic bladder, is unsuitable either for SNM or
IVES.
Nevertheless, SNM is a minimally invasive treatment
for chronic unobstructed urinary retention in women
[48] and which offers an effective therapeutic alternative
to CIC or indwelling catheterisation. After SNM, up to
72% of women could void spontaneously, with a mean
PVR of 100 mL, and half no longer needed CIC [49].
In a systematic review and meta-analysis [50] the overall
success rate for neurogenic lower urinary tract dysfunction was 68% for the test phase and 90% in those patients who received the implant. However, the methods
and data reported vary widely, with no clear differentiation between the indications for DU or DO. Randomised controlled trials are needed before drawing
conclusions on the value of SNM in neurogenic DU.
Surgical treatment for an acontractile detrusor
(functional detrusor myoplasty)
Detrusor myoplasty was ﬁrst described by Stenzl et al.
[51], and Gakis et al. [52] reported the long-term results
of latissimus dorsi detrusor myoplasty in neurogenic patients with detrusor acontractility, reporting that 71%
gained complete spontaneous voiding, with a mean
PVR of 25 mL. However, this interesting study represents the experience of only one group, not yet reproduced by others, and with few patients [24]. Hence we
should not be too optimistic about their results until larger trials with more patients are available.
326
Abdel Raheem, Madersbacher
Figure 1 Results from a 44-year-old woman who underwent several urethrotomies and urethroplasty, and presented with severe voiding
symptoms and a high PVR: (a) Uroﬂowmetry showed a prolonged ﬂuctuating pattern with a decreased Qmax and a PVR of 670 mL. (b)
The PFS showed a high PdetQmax of 64 cm H2O and a low Qmax of 4 mL/s. (c) VCUG showed a closed bladder neck due to functional and
anatomical reasons.
Voiding dysfunction in women: How to manage it correctly
327
Figure 2 A urodynamic study of a 91-year-old woman with mixed urgency and stress continence. (a) The urodynamic curves show DO
with weak detrusor contractions, accompanied by increased EMG activity (she tries to hold on voluntarily when urgency occurs), at
maximum cystometric bladder capacity only a minor increase of detrusor pressure, and voiding by abdominal straining. (b) On blocking
the bladder neck with the inﬂated balloon of the urodynamic catheter, there is a good detrusor contraction with a detrusor pressure
amplitude of 50 cm H2O, indicating that with increased outlet resistance (e.g. after sling implantation), a detrusor contraction can occur.
328
Future developments
DU could be a target for stem-cell therapy to restore the
contractile function of the bladder, but neither experimental nor clinical data are available. Direct electrical
stimulation of the acontractile detrusor was developed
by Merrill in the 1970s, with remarkable results [53],
but technical failures and infections were the main drawbacks. Moreover, in this period CIC became popular as
an effective method to empty the acontractile bladder. It
might be that with current technology and the improved
knowledge of bladder pathophysiology effective direct
electrostimulation of the bladder would be possible [54].
The treatment of BOO
Mechanical BOO
For iatrogenic BOO after treating stress urinary incontinence, e.g., after placing a MUS, if patients present with
voiding difﬁculty this can be managed with a short-term
(1 week) urethral catheterisation, and in most patients it
resolves spontaneously [55]. Only a few women (1%)
will develop chronic urinary retention. These patients
should be offered CIC or a suprapubic catheter, with a
close follow-up. If there is no improvement in symptoms, or in women who are unwilling to use CIC, division of the mesh should be offered. The tape should
be divided within the ﬁrst 3 weeks after surgery, to avoid
permanent features of urethral distortion resulting from
the progressive ﬁbroblastic reaction around the polypropylene mesh [56]. Obstruction occurring after a Burch
colposuspension could be treated by removing the
obstructing sutures ﬁxing the urethra to Cooper’s
ligament.
BOO due to POP is successfully treated with surgery
of the POP. Up to 74% of patients who had the cystocele repaired with anterior colporrhaphy or a polypropylene mesh repair had an improvement in their
voiding difﬁculties [57].
For a urethral stricture, urethral dilatation and internal urethrotomy have a high recurrence rate. With a rigid, narrow urethra some type of urethroplasty (a
vaginal inlay ﬂap, Blandy urethroplasty, or dorsal vaginal graft urethroplasty) might be necessary.
Functional BOO
For dyscoordinated voiding or ‘Hinman syndrome’, the
management of voiding includes biofeedback and bladder retraining programmes. Patients must be aware that
they have a false micturition behaviour. With the help of
a physiotherapist and biofeedback they must learn to relax the PFM during voiding. A suitable tool is the
recording of the EMG of the PFM by self-adhesive surface electrodes which are connected to earphones. The
Abdel Raheem, Madersbacher
patient is then acoustically informed whether she relaxes
or contracts the PFM during micturition [58]. In severe
cases (with a PVR of >50% of the functional bladder
capacity), at least initially, CIC should be offered.
For primary bladder neck obstruction, the use of ablockers might be useful. In women with functional
BOO who were treated with tamsulosin, Costantini
et al. [59] reported an improvement in voiding symptoms
in 71.4%, a decrease of the PVR in 62.5% and a 66.7%
improvement in both voiding and storage symptoms.
Transurethral incision of bladder neck, although advised by several authors, risks postoperative urinary
incontinence [60,61].
For DSD, CIC is still the standard treatment, thus by
passing the dyssynergic sphincter. For women unable to
use CIC an injection with botulinum toxin A (BTA) into
their striated sphincter is an option, but must be repeated every 3 months [62]. An injection with BTA for
treating neurogenic DSD was ﬁrst introduced by Dykstra and Sidi [63]. Up to 67% of patients reported an
improvement in voiding [64]. Other pharmacotherapy
for DSD is difﬁcult, e.g., striated muscle relaxants (e.g.
Baclofen) are effective only in high doses and are associated with a variety of side-effects which minimise their
overall usefulness. There is no study showing that oral
a-blockers improve DSD [62].
For patients with an established diagnosis of Fowler’s
syndrome, SNM has been shown to be most effective in
up to 72% [65].
Conclusions
Some 6% of women have voiding difﬁculties, which are
complex conditions and have several possible causes, the
most frequent of which is DU; BOO in females is relatively uncommon but a combination of DU and BOO
is possible.
As urinary symptoms have a poor correlation with
the underlying pathophysiology, urodynamic and imaging studies are crucial for the appropriate diagnosis,
especially to differentiate between DU and BOO, and
to determine the management.
A complete cure might not be possible for every woman with VD, and therefore relieving the symptoms and
minimising the long-term complications associated with
it should be the goal. With DU, behavioural therapy
should be offered ﬁrst to improve the condition. CIC
is important, especially for those with a high PVR.
The use of IVES and SNM as minimally invasive treatment options should be offered to women with some
preserved function of detrusor sensitivity and contractility. For mechanical BOO, abolishing the underlying
cause (obstructed sling or POP) improves or can even
normalise the condition. In women with functional
obstruction, behavioural therapy to eliminate false
micturitional behaviour is the ﬁrst line of treatment.
Voiding dysfunction in women: How to manage it correctly
For severe cases CIC is an option, indwelling catheterisation is the last resort, and urinary diversion should be
the rare exception for otherwise untreatable cases.
Conﬂict of interest statement
There is no conﬂict of interest.
Source of funding
None.
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